Electroconvulsive Therapy (ECT) Anaesthesia

Quick Answer

Electroconvulsive therapy (ECT) involves inducing a generalized tonic-clonic seizure under general anaesthesia for treatment of severe psychiatric disorders. Anaesthetic goals: Provide brief unconsciousness (2-5 minutes), muscle relaxation to prevent injury, and optimize seizure duration while minimizing physiological disturbance. Key physiological effects: Initial 10-15 second parasympathetic discharge (bradycardia/asystole possible), followed by 1-3 minute sympathetic surge (hypertension 40% above baseline, tachycardia 15% above baseline). Seizure requirements: EEG seizure duration 15-75 seconds optimal; <10 seconds or >120 seconds suboptimal. Induction agents: Methohexital (0.75-1.0 mg/kg) historically preferred; propofol (0.75-1.5 mg/kg) commonly used but may shorten seizure; etomidate (0.15-0.3 mg/kg) for seizure-resistant patients. Muscle relaxants: Suxamethonium (0.5-1.0 mg/kg) standard; rocuronium (0.6 mg/kg) with sugammadex reversal alternative. Monitoring: EEG essential for seizure confirmation; EMG and direct observation also used. Contraindications: No absolute contraindications; relative include recent MI, increased intracranial pressure, unstable aneurysm, and pregnancy. [1-25]

Indications and Mechanism of ECT

Indications for ECT

Primary Indications:

• Major Depressive Disorder: Treatment-resistant or requiring rapid response (high suicidality)
• Bipolar Disorder: Severe mania or depressive episodes
• Schizophrenia: Acute exacerbations, treatment-resistant cases, catatonia
• Catatonia: All forms (malignant, neuroleptic-induced, idiopathic)
• Neuroleptic Malignant Syndrome: Alternative treatment
• Parkinson's Disease: Severe motor symptoms, "on-off" phenomena
• Status Epilepticus: Paradoxical use to terminate seizures (rare)

Special Populations:

• Pregnancy: Considered safe in all trimesters when indicated
• Elderly: Often preferred over medication due to reduced side effects
• Children/Adolescents: Rare, for severe treatment-resistant conditions
• Emergency settings: Rapid response required (suicidality, catatonia, NMS)

Mechanism of Action

Neurochemical Hypothesis:

• Increased release of neurotransmitters: serotonin, dopamine, norepinephrine, acetylcholine
• Upregulation of neurotrophic factors (BDNF, NGF)
• Enhanced neuroplasticity and synaptogenesis
• Modulation of hypothalamic-pituitary-adrenal axis
• Reduction in pro-inflammatory cytokines

Neurophysiological Changes:

• Increased cerebral blood flow during seizure
• Temporary blood-brain barrier disruption
• Enhanced glucose metabolism in limbic structures
• Increased slow-wave activity on EEG post-treatment

Antidepressant Effects:

• Therapeutic effect requires multiple treatments (typically 6-12 sessions)
• Improvement often seen after 4-6 treatments
• Mechanism distinct from spontaneous seizures (controlled, therapeutic context)
• Seizure quality (duration, EEG pattern) correlates with outcome

Physiological Effects of ECT

Cardiovascular Response

Phases of Cardiovascular Response:

Phase 1 - Parasympathetic Discharge (0-15 seconds):

• Mechanism: Initial vagal response to electrical stimulus
• Bradycardia: Heart rate may drop 20-50%
• Asystole: Brief periods (3-10 seconds) common; usually self-limiting
• Hypotension: Brief drop in blood pressure
• Management: Usually requires no treatment; atropine rarely needed
• Severe cases: Asystole >10 seconds may require glycopyrrolate/atropine

Phase 2 - Sympathetic Surge (15 seconds - 3 minutes):

• Mechanism: Catecholamine release from adrenal medulla and sympathetic terminals
• Tachycardia: 15-30% increase above baseline
• Hypertension: Systolic pressure may increase 20-50 mmHg (up to 40% above baseline)
• Cardiac output: Increased
• Myocardial oxygen demand: Significantly increased
• Arrhythmias: Premature ventricular contractions, supraventricular tachycardia

Phase 3 - Resolution (3-10 minutes):

• Gradual return to baseline hemodynamics
• Some patients may experience post-ictal bradycardia
• Hypotension uncommon but possible

Monitoring Requirements:

• Continuous ECG throughout procedure
• Blood pressure every minute during and after seizure
• Defibrillator immediately available
• Consider arterial line for high-risk cardiac patients

Cerebrovascular Effects

Cerebral Blood Flow:

• Marked increase during seizure (up to 400% above baseline)
• Reactive hyperemia post-seizure
• Coupled with increased metabolic demand
• Risk of ischemia if demand exceeds supply

Intracranial Pressure:

• Transient elevation during seizure
• Concern in patients with space-occupying lesions
• Generally well-tolerated in normal brain

Neurochemical Changes:

• Increased oxygen extraction
• Transient lactate accumulation
• pH changes in cerebral tissue

Cognitive Effects:

• Anterograde amnesia common (expected effect)
• Retrograde amnesia (variable, usually limited)
• Confusion post-ictal (usually resolves within hours)
• Memory deficits typically improve over weeks

Respiratory Effects

During Seizure:

• Apnea common during tonic phase
• Irregular respirations during clonic phase
• Oxygen consumption increased
• Lactic acidosis from anaerobic metabolism

Post-Seizure:

• Snoring or partial airway obstruction common
• Hypoxemia possible without supplemental oxygen
• Risk of aspiration if inadequate airway protection
• Laryngospasm rare but possible

Management:

• Preoxygenation essential (3-5 minutes with 100% O2)
• Continue oxygenation during and after seizure
• Suction available for secretions
• Bag-mask ventilation if respiratory depression

Musculoskeletal Effects

Without Muscle Relaxation:

• Violent tonic-clonic movements
• Risk of fractures (vertebral compression, long bones)
• Dental damage, tongue biting
• Soft tissue injuries
• Dislocations

With Adequate Relaxation:

• Minimal visible movement
• "Modified" ECT standard practice since 1950s
• Some blanching of toe/foot observed
• Masseter muscle contraction may persist

Anaesthetic Management

Preoperative Assessment

Essential Evaluation:

• Airway assessment: Mallampati, thyromental distance, neck mobility
• Cardiovascular history: IHD, arrhythmias, hypertension, CHF
• Neurological history: Seizures, strokes, increased ICP
• Medications: Current psychiatric medications, anticoagulants
• NPO status: Minimum 6 hours for solids, 2 hours for clear liquids
• Vital signs: Baseline blood pressure, heart rate

Investigations:

• ECG (age >40 or cardiac history)
• Electrolytes (K+, Mg2+, Ca2+ for cardiac patients)
• FBC if anemia suspected
• CXR if indicated
• Pregnancy test if applicable

Risk Stratification:

• ASA 1-2: Standard management
• ASA 3: Optimize comorbidities; consider prophylactic medications
• ASA 4: Consult cardiology/neurology; individualized risk-benefit

Anaesthetic Technique

Goals:

1. Rapid loss of consciousness
2. Brief duration (2-5 minutes)
3. Muscle relaxation to prevent injury
4. Rapid emergence
5. Minimal interference with seizure
6. Hemodynamic stability

Positioning:

• Supine on stretcher
• Head slightly elevated or neutral
• Tourniquet on one limb (for motor monitoring)
• Bite block in place before stimulus
• Apply EEG electrodes

Standard Monitoring:

• Continuous ECG
• Non-invasive blood pressure (minute-by-minute)
• Pulse oximetry
• Capnography (if using supplemental airway)
• EEG (mandatory for seizure confirmation)
• EMG (motor seizure monitoring)

Induction Agents

Methohexital (Gold Standard):

• Dose: 0.75-1.0 mg/kg IV
• Onset: 15-30 seconds
• Duration: 5-7 minutes
• Advantages: Proven efficacy, does not interfere with seizure, rapid recovery
• Disadvantages: Burning on injection, hiccups, myoclonus, excitatory phenomena
• Availability: Limited in some countries

Propofol (Most Commonly Used):

• Dose: 0.75-1.5 mg/kg IV (higher doses may suppress seizure)
• Onset: 15-30 seconds
• Duration: 3-5 minutes
• Advantages: Rapid, smooth emergence; antiemetic; widely available
• Disadvantages: Dose-dependent seizure shortening (0.75 mg/kg preferred); pain on injection
• Evidence: Effective if dose kept low; may require higher electrical stimulus

Etomidate:

• Dose: 0.15-0.3 mg/kg IV
• Onset: 15-30 seconds
• Duration: 5-10 minutes
• Advantages: Does not suppress seizures (may prolong); useful in seizure-resistant patients
• Disadvantages: Adrenal suppression with repeated doses; myoclonus; pain on injection
• Indication: Patients with high seizure threshold or prior inadequate seizures

Thiopentone:

• Dose: 1.5-2.5 mg/kg IV
• Limited use: May excessively prolong recovery
• Historical significance: Previously widely used

Ketamine:

• Dose: 0.5-1.0 mg/kg IV
• Emerging role: Potential antidepressant synergy
• Concerns: Prolonged emergence; hallucinations; hemodynamic stimulation
• Evidence: Mixed results on efficacy; reserved for refractory cases

Volatile Anaesthesia:

• Sevoflurane mask induction possible
• Rarely used; time-consuming
• Useful if IV access difficult

Muscle Relaxants

Succinylcholine (Suxamethonium) - Standard:

• Dose: 0.5-1.0 mg/kg IV (often 0.5-0.75 mg/kg sufficient)
• Onset: 30-60 seconds
• Duration: 3-5 minutes
• Advantages: Rapid, reliable, short duration, excellent intubating conditions
• Disadvantages: Requires refrigerator; contraindications (see below)
• Defasciculation: Optional with small dose non-depolarizer (rarely done)

Rocuronium (Alternative):

• Dose: 0.6 mg/kg IV for intubation-level block
• Reversal: Sugammadex 16 mg/kg (rapid)
• Advantages: No contraindications like suxamethonium
• Disadvantages: Longer duration; requires sugammadex (expensive); monitoring needed
• Indication: Suxamethonium contraindicated

Mivacurium (Alternative):

• Dose: 0.15-0.2 mg/kg IV
• Duration: 15-20 minutes
• Advantages: Short-acting non-depolarizer; spontaneous recovery
• Disadvantages: Histamine release; prolonged vs suxamethonium
• Limited availability: Not available in all countries

Atracurium/Cisatracurium:

• Generally too long-acting for routine ECT
• May be used if rocuronium/sugammadex unavailable
• Requires ventilation until recovery

Contraindications to Suxamethonium

Absolute Contraindications:

• Malignant hyperthermia: Risk of triggering MH crisis
• Personal or family history of MH
• Duchenne muscular dystrophy: Risk of rhabdomyolysis, hyperkalemia, cardiac arrest
• Acute burn >24 hours old: Risk of hyperkalemia
• Denervation injuries: Risk of hyperkalemia
• Upper motor neuron lesions: Risk of hyperkalemia
• Severe skeletal muscle trauma: Risk of hyperkalemia

Relative Contraindications:

• Pseudocholinesterase deficiency: Prolonged apnea
• History of severe muscle pain: Post-suxamethonium myalgia
• Increased intracranial pressure: Transient increase (minimal with dose used)
• Open eye injury: Transient pressure increase
• Bradycardia: Risk of asystole (pre-treat with atropine/glycopyrrolate)

Airway Management

Standard Approach:

• Spontaneous ventilation: Most common
• Supplemental oxygen: Via face mask or nasal cannula
• Bite block: Essential to prevent dental/oral injury
• Suction: Immediately available for secretions

Adjuncts:

• Nasopharyngeal airway: If airway obstruction occurs
• Oral airway: Generally avoided (risk of bite block displacement)
• LMA: Consider if difficult airway or prolonged procedure
• ETT: Rarely needed; reserved for aspiration risk or failed airway

Emergence:

• Position patient lateral if drowsy
• O2 until fully awake (SpO2 >94% on room air)
• Monitor for airway obstruction
• Suction secretions before extubation if ETT used

Stimulus Dosing and Seizure Monitoring

Seizure Threshold Determination

Initial Treatment:

• Age-based dosing: Common starting point
  • Age <40: 100-200 mC (millicoulombs)
  • Age 40-60: 200-300 mC
  • Age >60: 300-500 mC
• Stimulus titration: Start low and increase until seizure
• Subconvulsive stimulus: No motor or EEG seizure
• Convulsive stimulus: Adequate seizure induced

Subsequent Treatments:

• Dose adjustment: Based on previous seizure quality
• Seizure duration: Target 15-75 seconds (EEG)
• Suprathreshold dosing: 50-100% above threshold typically used
• Right unilateral vs bilateral: Dosing differs (lower for unilateral)

Seizure Monitoring

EEG (Gold Standard):

• Tonic phase: High-frequency, low-amplitude activity
• Clonic phase: High-amplitude polyspike activity
• Post-ictal: Slowing, then return to baseline
• Duration: Measure from initial spike to final slow wave
• Quality markers: Polyspike activity, rhythmicity, amplitude

Motor Seizure (EMG):

• Tourniquet technique: Isolate limb from muscle relaxant
• Observation: Watch for toe/finger movement
• Duration: Shorter than EEG seizure (tetanic fade)
• Correlation: Motor duration ~80% of EEG duration

Acceptable Seizure Parameters:

• EEG duration: 15-75 seconds optimal
• <10 seconds: Subtherapeutic; increase dose
• >120 seconds: Prolonged; may require termination
• Motor duration: At least 10 seconds desirable
• EEG endpoint: Return to pre-stimulus activity

Managing Seizure Characteristics

Inadequate Seizures (<10 seconds):

• Increase stimulus dose: 50-100% increments
• Optimize physiological parameters: Hyperventilate pre-induction
• Sleep deprivation: May lower threshold
• Caffeine: Pre-treatment may enhance seizure
• Change induction agent: Etomidate instead of propofol
• Medication review: Reduce anticonvulsants if possible

Prolonged Seizures (>120 seconds):

• Midazolam: 1-2 mg IV to terminate
• Propofol: Additional dose
• Post-ictal care: Extended monitoring; risk of delayed awakening
• Investigation: Check electrolytes, especially magnesium
• Medication adjustment: May need dose reduction

Special Populations and Considerations

Cardiovascular Disease

Hypertension:

• Continue antihypertensives day of treatment
• Pre-treatment with labetalol or esmolol if severe
• Monitor for exaggerated hypertensive response
• Risk of myocardial ischemia if untreated

Coronary Artery Disease:

• Optimization before ECT
• Consider pre-treatment with beta-blocker or labetalol
• Nitroglycerin available for chest pain
• Post-treatment monitoring in recovery

Arrhythmias:

• Atrial fibrillation: Rate control important
• PVCs common post-seizure; usually benign
• Defibrillator immediately available
• ACLS protocols if sustained arrhythmia

Heart Failure:

• Volume status optimization
• Careful fluid management
• Monitor for pulmonary edema
• Consider cardiology consultation

Neurological Conditions

Increased Intracranial Pressure:

• Space-occupying lesions: Relative contraindication
• Consider dexamethasone pre-treatment
• Monitor neurological status post-treatment
• Consult neurosurgery if concern

Seizure Disorders:

• Continue anticonvulsants (may increase threshold)
• Higher stimulus doses often required
• Risk of prolonged seizures
• Monitor for status epilepticus

Cerebrovascular Disease:

• Recent stroke (<3 months): Delay if possible
• Unstable aneurysm: Relative contraindication
• Optimize blood pressure control
• Nimodipine for vasospasm risk

Pregnancy

Safety:

• Safe in all trimesters when indicated
• Modified ECT standard (muscle relaxation essential)
• Left uterine displacement after 20 weeks
• Fetal monitoring if viable fetus
• Obstetric consultation recommended

Considerations:

• Aspiration risk (delayed gastric emptying)
• Consider H2 antagonist, metoclopramide pre-treatment
• Airway edema in third trimester
• Aspiration prophylaxis (cricoid pressure if needed)
• Higher risk of arrhythmias

Complications:

• Risk of preterm labor (low)
• Fetal bradycardia during maternal asystole (benign)
• Uterine contractions post-treatment (monitor)

Elderly Patients

Advantages:

• Often better tolerated than medications
• Rapid response beneficial
• Lower suicide risk during treatment

Considerations:

• Higher seizure threshold
• Greater cognitive side effects
• Multiple comorbidities
• Fracture risk with osteoporosis
• Prolonged confusion post-treatment

Management:

• Lower stimulus dosing initially
• Conservative anaesthetic doses
• Extended recovery monitoring
• Fall prevention post-treatment
• Memory aids and support

Children and Adolescents

Indications:

• Catatonia
• Severe depression with suicidality
• Mania with dangerous behavior
• Treatment-resistant psychosis
• Neuroleptic malignant syndrome

Considerations:

• Parental/guardian consent required
• Age-appropriate preparation
• Psychological support
• School accommodation during course
• Developmental monitoring

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Peoples:

Indigenous Australians experience significant mental health disparities, with higher rates of depression, anxiety, and psychological distress compared to non-Indigenous populations. The historical and ongoing impacts of colonization, forced removal of children, and intergenerational trauma contribute to elevated psychiatric morbidity. Despite this higher burden of mental illness, access to ECT services is often limited by geographic factors, with many Indigenous patients in remote and rural areas far from specialized psychiatric facilities.

The stigma associated with mental illness and ECT itself may be pronounced in some Aboriginal communities, where traditional understandings of health and illness differ from Western biomedical models. Engagement with Aboriginal Health Workers and community leaders is essential for culturally safe delivery of ECT. These cultural brokers can facilitate understanding of the procedure, support informed consent processes, and help manage community perceptions.

Cardiovascular comorbidities, including hypertension, diabetes, and renal disease, are more prevalent among Indigenous Australians and increase the risks associated with ECT. The autonomic responses to seizure induction pose particular challenges in patients with existing cardiovascular disease. Pre-ECT optimization and close monitoring during the sympathetic surge phase are essential.

Follow-up after ECT treatment courses may be challenging in remote settings where psychiatric follow-up and monitoring for relapse are limited. Collaborative care models involving telepsychiatry, Aboriginal Mental Health Workers, and local primary care providers help ensure continuity of care and early detection of relapse.

Māori Health Considerations:

Māori experience elevated rates of mental health conditions, with higher suicide rates, depression, and psychosis than non-Māori populations. However, Māori are less likely to access specialist mental health services and may present later with more severe illness. This delayed presentation can mean that ECT is required for more acute, severe conditions.

Cultural concepts of mental health and wellbeing in Te Ao Māori may not align with Western psychiatric diagnoses, and some Māori may prefer traditional healing approaches (rongoa Māori) alongside or instead of Western treatments. Culturally safe ECT practice requires acknowledging and respecting these preferences while providing evidence-based care when ECT is indicated. Whānau involvement in treatment decisions is fundamental, and discussions regarding ECT should include extended family members where the patient wishes.

The physical health comorbidities common among Māori, including obesity, diabetes, and cardiovascular disease, create higher anaesthetic risk for ECT. Sleep apnoea is also more prevalent, increasing the risk of airway obstruction during the post-ictal period. Careful airway assessment and post-procedure monitoring are particularly important.

For Māori living in rural areas, accessing ECT may require travel to urban centers, creating disruption to whānau and employment. Community-based ECT services and outreach psychiatry help address these barriers. Follow-up care after ECT courses, including continuation pharmacotherapy and relapse prevention, requires robust systems that may not exist in rural settings.

ANZCA Exam Focus

Common Viva Topics

Physiology:

• Describe the cardiovascular response to ECT seizure
• Explain the phases of autonomic discharge during ECT
• Discuss the mechanism of action of ECT
• How does seizure quality affect therapeutic efficacy?

Pharmacology:

• Compare methohexital, propofol, and etomidate for ECT
• What are the contraindications to suxamethonium?
• How do you manage a patient with prolonged seizure (>120 seconds)?
• What is the role of rocuronium and sugammadex in ECT?

Clinical Management:

• How would you anaesthetize a patient for ECT?
• Describe your airway management for ECT
• How do you monitor seizure quality?
• What are the considerations for ECT in pregnancy?

Assessment Content

SAQ 1: ECT Physiology and Pharmacology (20 marks)

A 55-year-old female is scheduled for her first ECT treatment for severe treatment-resistant depression with suicidal ideation.

a) Describe the cardiovascular physiological changes during an ECT-induced seizure. (8 marks)

b) What are the key considerations in choosing an induction agent for ECT? Compare methohexital and propofol. (6 marks)

c) What monitoring is essential during ECT, and what constitutes an adequate seizure? (6 marks)

Model Answer:

a) Cardiovascular changes during ECT:

Phase 1 - Parasympathetic (0-15 seconds):

• Initial vagal discharge from electrical stimulus (1 mark)
• Bradycardia (20-50% drop in HR) (1 mark)
• Brief asystole (3-10 seconds) may occur (1 mark)
• Usually self-limiting; rarely requires treatment (1 mark)

Phase 2 - Sympathetic (15 seconds - 3 minutes):

• Massive catecholamine release (1 mark)
• Tachycardia (15-30% increase in HR) (1 mark)
• Hypertension (systolic may increase 40% above baseline) (1 mark)
• Increased myocardial oxygen demand (1 mark)

b) Induction agent considerations:

Key requirements:

• Rapid onset and offset (1 mark)
• Minimal interference with seizure (1 mark)
• Hemodynamic stability (1 mark)

Comparison:

• Methohexital: 0.75-1.0 mg/kg; proven efficacy; does not suppress seizure; gold standard; limited availability (1.5 marks)
• Propofol: 0.75-1.5 mg/kg; widely available; rapid recovery; dose-dependent seizure shortening; use lower dose (1.5 marks)

c) Essential monitoring and adequate seizure:

Monitoring:

• Continuous ECG (arrhythmias common) (1 mark)
• Blood pressure monitoring (minute-by-minute) (1 mark)
• Pulse oximetry (1 mark)
• EEG (mandatory for seizure confirmation) (1 mark)
• EMG/motor observation (1 mark)

Adequate seizure:

• EEG duration 15-75 seconds (1 mark)
• At least 10 seconds motor activity (tourniquet technique) (1 mark)
• High-quality EEG: polyspike activity, rhythmicity (1 mark)

SAQ 2: Complications and Special Populations (20 marks)

A 45-year-old male with a history of Duchenne muscular dystrophy requires ECT for catatonia. He weighs 70kg.

a) What specific concerns does this patient's history raise regarding muscle relaxant choice? (4 marks)

b) What is the pathophysiology of the adverse reaction to suxamethonium in this condition? (4 marks)

c) Outline your anaesthetic management, including induction agent, muscle relaxant, and specific precautions. (8 marks)

d) What other conditions share this contraindication to suxamethonium? (4 marks)

Model Answer:

a) Concerns with Duchenne muscular dystrophy:

• Suxamethonium absolutely contraindicated (2 marks)
• Risk of rhabdomyolysis and hyperkalemic cardiac arrest (1 mark)
• Need for alternative muscle relaxant strategy (1 mark)

b) Pathophysiology of suxamethonium reaction:

• Denervated muscles upregulate extra-junctional nicotinic receptors (2 marks)
• Suxamethonium depolarizes all muscle cells (not just neuromuscular junction) (1 mark)
• Massive potassium release from muscle cells (1 mark)

c) Anaesthetic management:

Induction:

• Methohexital 0.75-1.0 mg/kg or propofol 0.75 mg/kg (2 marks)
• Standard monitoring plus extended ECG monitoring (1 mark)

Muscle relaxant:

• Rocuronium 0.6 mg/kg (not suxamethonium) (2 marks)
• Reverse with sugammadex 16 mg/kg at procedure end (2 marks)

Precautions:

• Defibrillator immediately available (1 mark)
• Monitor for cardiac arrhythmias (cardiomyopathy common) (1 mark)
• Extended recovery monitoring (respiratory muscle weakness) (1 mark)

d) Other suxamethonium contraindications:

• Malignant hyperthermia (personal/family history) (1 mark)
• Acute burns >24 hours old (1 mark)
• Denervation injuries/upper motor neuron lesions (1 mark)
• Severe skeletal muscle trauma/rhabdomyolysis (1 mark)

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